Preliminary studies have demonstrated that Long-Evans rats treated with lead (200 mg/kg/day) during development (days 2-30) were significantly more polydipsic after lithium administration than were nonlead-treated, paired controls. This change persists until the animals are at least six months of age. The animals tested showed no other consistent behavioral, biochemical or pathological alteration. The involvement of the peripheral renin-angiotensin system, known to be elevated by lithium, will be investigated in lead and control animals using radioimmunoassay methodology. Other known dipsogenic agents will be administered by various routes to determine if infantile lead exposure causes increased polydipsia to other agents, either alone or after lithium pretreatment. Since central dopaminergic neurons are known to be essential to lithium-induced polydipsia, lead-treated and control rats will be depleted of catecholamines in the central nervous system using 6-hydroxydopamine. The alterations in drinking responses to lithium and other dipsogenic agents will be measured after generalized and specific catecholamine depletions. These studies provide a model for the study of lead toxicity on the central nervous system of developing rats that is extremely reproducible, easily quantifiable, and relevant to both basic and clinical aspects of lead poisoning.